Tumor-associated neutrophils strongly inhibited IL-17 production by γδ T cells via the induction of oxidative stress, thereby exerting antitumoral activity in the tumor microenvironment.124 On the other hand, IL-17-producing γδ T cells were found to expand neutrophils in a granulocyte colony-stimulating factor (G-CSF)-dependent manner in a breast cancer model, which then actually suppressed CD8 T cell responses, thereby promoting metastasis formation.80 This evidence concerns the gene CSF3 and breast cancer.